Severe Peptic Ulcer Disease Research Articles

Laparoscopic management of benign gastric outlet obstruction: a case series with review of literature

Surgery for peptic ulcer disease has since long become a thing of the past, in the era of proton pump inhibitors. Today, it is difficult to believe that these were common operations about 6-7 decades ago. Such has been the impact of proton pump inhibitors (PPI), that, surgery for peptic ulcer has been relegated to the realms of history. However, even in present day, in some rare clinical situations, surgeons may have to resort to surgery for patients suffering from peptic ulcer disease. Herein, we present our experience of laparoscopic surgical management of one of those rare clinical scenarios related to severe peptic ulcer disease. The clinical condition in discussion is gastric outlet obstruction caused by severe peptic ulcer disease in the first part of duodenum. We identified 8 patients (7 males and 1 female) who underwent laparoscopic vagotomy with gastrojejunostomy for benign gastric outlet obstruction, at our institution, operated upon by a single surgeon, between 2004 to 2023. All patients had undergone oesophago-gastro-duodenoscopy (OGD scopy), and contrast enhanced computerised tomography (CECT) of the abdomen. The patients were analysed for age, sex, symptoms, pre-operative evaluation, morbidity/mortality and functional outcomes. They were also reviewed to examine the length of stay, length of procedure, complications and recurrent symptoms on follow-up.

S4297 Acquired Double Pylorus: A Rare Endoscopic Finding of Severe Peptic Ulcer Disease

S4297 Acquired Double Pylorus: A Rare Endoscopic Finding of Severe Peptic Ulcer Disease

S3543 An Unusual Complication of Peptic Ulcer Disease

Introduction: In patients with severe peptic ulcer disease (PUD), perforation is a serious complication, often presenting with acute abdominal pain. Perforation occurs in approximately 5% of patients with PUD over their lifetime. Although fistulas have been reported as a potential complication of postoperative perforated peptic ulcer disease, we present a unique case of antral-abscess fistula complicated by duodenal adenocarcinoma. Case Description/Methods: A 57-year-old female presented to the hospital with a chief complaint of epigastric pain. The patient had a history of perforated gastric ulcer status post graham patch repair. Computed Tomography (CT) of abdomen revealed remote gastric perforation with chronic fistulous connection between the gastric antrum and an abscess along the superior margin of the gastric antrum, underneath the left liver. Upper GI endoscopy revealed diffuse mildly erythematous mucosa without bleeding in the stomach as well as non-bleeding large cratered chronic appearing duodenal ulcer with a clean ulcer base (Forrest Class III) in the duodenal bulb involving more than 90% of the duodenal circumference, causing narrowing at the duodenal sweep and 2nd portion of duodenum. There were multiple ulcer/mucosal changes spots of bluish/reddish concerning for non-bleeding visible vessel and fistula given the severity of the ulcer/mucosal changes. Subsequent duodenal ulcer biopsy revealed necrotic tissue with infiltrating cells which were significant for adenocarcinoma of the duodenum (Figure). Discussion: To our knowledge, this is the first report demonstrating antral stomach-abscess fistula with concomitant evidence of duodenal adenocarcinoma after perforated peptic ulcer disease. With this report, we not only aim to shed light on this unique complication but also to spark the scientific community to further investigate potential associations of duodenal adenocarcinoma including peptic ulcer disease.Figure 1.: Endoscopy of duodenum demonstrating ulcerations concerning for non-visible bleeding vessels and fistula.

S2307 A Case of Severe Peptic Ulcer Disease and Bleeding Duodenal Ulcer in a COVID-19 Patient

Introduction: COVID-19 is described as a respiratory illness, with primary symptoms of fever, cough, and shortness of breath. However, greater than 10% of COVID-19 patients experience GI symptoms as well, typically nausea, vomiting, and diarrhea. We present a case of an unusually severe, acute upper GI bleed in a patient with COVID-19, who successfully underwent endoscopic intervention. Case Description/Methods: A 90-year-old male presented to the ED with altered mental status and decreased appetite. He was found to be hypoxic, requiring 15L of oxygen. Labs were significant for a hemoglobin of 21.4 g/dl, consistent with known polycythemia, and a positive COVID-19. On day 4, the patient became hypotensive, hemoglobin dropped from 17.3 to 11 g/dl, and melena was reported. He was given 1 unit of RBCs and started on levophed and a high dose PPI. The GI team was weighing the risk of endoscopy when his hemoglobin dropped to 9 g/dl that same day, and the decision was made to perform urgent EGD. EGD demonstrated multiple ulcerations throughout the stomach, the largest of which measured 18 mm, with none actively bleeding but several containing pigment. The duodenal bulb had a large area of deep ulceration with a visible vessel (Forrest IIa ulcer) not actively bleeding. It was successfully treated with epinephrine injection and four hemostatic clips. Over the course of his stay, the patient’s hemoglobin stabilized and he was weaned to 2L oxygen. H. pylori returned positive, and the patient was discharged on day 15 with an oral PPI and instructions to follow up with his PCP for H. pylori eradication. Discussion: The relationship between COVID-19 and upper GI bleeds has been established, as SARS-Cov-2 RNA has been identified in both fecal samples and peptic ulcers in COVID-positive patients. However, this patient with multiple ulcers extending through the stomach and duodenum represents an unusual and severe case, distinct in both number and location. Additionally, while H. pylori is already believed to be a predictor of GI symptoms, considering its ability to upregulate ACE-2 receptors in the GI tract, this case points to H. Pylori as a possible predictor of acute GI bleeds in COVID-positive patients as well. Finally, while scoping COVID-positive patients remains a topic of debate, considering the risk of exposure to patients and staff, this report of the successful treatment of a 90-year-old with impending hemodynamic collapse supports the case for early intervention.

Агрессивные и протективные факторы желудочного сока у больных со стенозом пилородуоденальной зоны язвенного генеза

Цель: оценить агрессивные и протективные свойства желудочного сока у больных со стенозом пилородуоденальной зоны язвенного генеза в зависимости от его степени. Материалы и методы. В отделении хирургии органов пищеварения ГУ «Институт гастроэнтерологии НАМН У­краины» за 2014–2019 годы обследовано 157 больных с различной степенью стеноза пилородуоденальной зоны язвенного генеза. Из них для изучения желудочной кислото- и слизепродукции было отобрано 92 пациента с компенсированным и субкомпенсированным стенозом, среди которых 71 мужчина, 21 женщина в возрасте от 38 до 56 лет, средний возраст (45,3 ± 5,2) года. Больные были разделены на 2 группы в зависимости от степени стеноза: 1 группа — 57 больных с компенсированным стенозом, 2 группа — 35 больных с субкомпенсированным стенозом. Контрольную группу составили 20 практически здоровых лиц. В желудочном содержимом определяли: уровень pH, концентрацию пепсина, гликопротеинов, гексозаминов, фукозы, сиаловых кислот. Результаты. Анализ изучения уровней кислото- и слизепродукции у больных со стенозом пилородуоденальной зоны различной выраженности показал, что у пациентов с субкомпенсированным стенозом отмечалось увеличение частоты гиперацидной секреции на 21,1 % (р < 0,05), существенное повышение уровня пепсина (р < 0,05), уменьшение концентрации общих гликопротеинов (р < 0,05) (за счет существенного уменьшения концентрации фукозы и гексозаминов) по сравнению с пациентами с компенсированным стенозом, которым была более свойственна нормацидная секреция. Полученные нами данные о дисбалансе факторов агрессии и защиты желудочного содержимого позволили нам сформировать различные адаптационно-компенсаторные варианты их соотношения: 1 (гиперреактивный) — одно­временное повышение факторов агрессии и защиты; 2 (компенсаторный) — повышение уровня агрессивных факторов, нормальная концентрация защитных факторов; 3 (декомпенсаторный) — повышение уровня агрессивных факторов, снижение уровня факторов защиты. Выводы. Выявлено, что прогрессирование степени стеноза пилородуоденальной зоны язвенного генеза из компенсированного в субкомпенсированный сопровождается достоверным преобладанием факторов агрессии над факторами защиты желудочного сока и истощением функциональных возможностей слизепродуцирующего аппарата желудка. В результате выделения трех вариантов соотношения факторов агрессии и защиты желудочного сока (гиперреактивный, компенсаторный, декомпенсаторный) установлено, что декомпенсаторный вариант достоверно чаще встречается у пациентов с субкомпенсированным стенозом пилородуоденальной зоны, а значит, риск прогрессирования степени стеноза у таких больных значительно выше по сравнению с другими вариантами соотношений. Обнаруженные варианты соотношений факторов агрессии и защиты у пациентов со стенозом дают возможность дифференцированного подхода к выбору тактики лечения (мини-инвазивного эндоскопического или комбинированного эндо- и лапароскопического метода).

Anti-inflammatory activity of 2-((3-(chloromethyl)benzoyl)oxy)benzoic acid in LPS-induced rat model

IntroductionSalicylic acid derivate is very popular for its activity to suppress pain, fever, and inflammation. One of its derivatives is acetylsalicylic acid (ASA) which has been reported repeatedly that, as a non-steroidal anti-inflammatory drug (NSAID), it has a cardioprotective effect. Although ASA has various advantages, several studies have reported that it may induce severe peptic ulcer disease. We recently synthesized a new compound derived from salicylic acid, namely 2-((3-(chloromethyl)benzoyl)oxy)benzoic acid (3-CH2Cl) which still has the benefit of acetylsalicylic acid as an analgesic and antiplatelet, but lacks its harmful side effects (Caroline et al., 2019). In addition, in silico studies of 3-CH2Cl showed a higher affinity towards protein receptor cyclooxygenase-2 (COX-2; PDB: 5F1A) than ASA. We hypothesized that 3-CH2Cl inhibits the COX-2 activity which could presumably decrease the inflammatory responses. However, no knowledge is available on the anti-inflammatory response and molecular signaling of this new compound. Hence, in this study, we investigated the potential functional relevance of 3-CH2Cl in regulating the inflammatory response in lipopolysaccharide (LPS)-induced rats. The results of this study show that this compound could significantly reduce the inflammatory parameter in LPS-induced rats. Material and methodsRats were induced with LPS of 0.5 mg/kg bw intravenously, prior oral administration with vehicle (3% Pulvis Gummi Arabicum / PGA), 500 mg/60 kg body weight (bw; rat dosage converted to human) of 3-CH2Cl and ASA. The inflammatory parameters such as changes in the temperature of septic shock, cardiac blood plasma concentrations of IL-1β and TNF-α (ELISA), blood inflammation parameters, white blood cell concentrations, and lung histopathology were observed. Meanwhile, the stability of 3-CH2Cl powder was evaluated. ResultAfter the administration of 500 mg/60 kg bw of 3-CH2Cl (rat dosage converted to human) to LPS-induced rats, we observed a significant reduction of both TNF-α (5.70+/-1.04 × 103 pg/mL, p=<0.001) and IL-1β (2.32+/-0.28 × 103 pg/mL, p=<0.001) cardiac blood plasma concentrations. Besides, we found a reduction of white blood cell concentration and the severity of lung injury in the 3-CH2Cl group compared to the LPS-induced rat group. Additionally, this compound maintained the rat body temperature within normal limits during inflammation, preventing the rats to undergo septic shock, characterized by hypothermic (t = 120 min.) or hyperthermic (t = 360 min) conditions. Furthermore, 3-CH2Cl was found to be stable until 3 years at 25°C with a relative humidity of 75 ± 5%. Conclusion3-CH2Cl compound inhibited inflammation in the LPS-induced inflammation response model in rats, hypothetically through binding to COX-2, and presumably inhibited LPS-induced NF-κβ signaling pathways. This study could be used as a preliminary hint to investigate the target molecular pathways of 3-CH2Cl as a novel and less toxic therapeutical agent in alleviating the COX-related inflammatory diseases, and most importantly to support the planning and development of clinical trial.

SAT-121 Secretin Stimulation Test in a Patient Receiving Proton PUMP Inhibitor Therapy- to Do or Not to Do?

Introduction:Complications of gastrinoma cause increase in mortality in patients with MEN syndrome. There are concerns that secretin stimulation test (SST) can produce false positive results in the setting of proton pump inhibitor (PPI) use. However, withholding the PPI treatment in a patient with severe peptic ulcer disease can be potentially unsafe. There is also a theoretical concern that abrupt withdrawal of PPI will cause a surge in gastrin. Here we discuss a case where SST yielded impressive results despite the use of PPI.Case report:78 y.o. Caucasian male presented in December 2018 with chronic nausea, vomiting, diarrhea of 5-year duration. Further evaluation showed severe esophagitis with strictures, multiple gastric and duodenal ulcers and he was initiated on PPI. He also had h/o hyperparathyroidism diagnosed 2 years ago s/p parathyroidectomy (2 of 4 parathyroid glands removed) and one kidney stone in his late 20s and early 70s. He had no family history of any endocrine issues. Physical examination was unremarkable. Labs were significant for gastrin levels (nl <100 pg/mL) of 375 pg/mL in 6/2016 and 219 pg/mL in 11/2018. SST was performed on 12/22/2018 which showed gastrin levels as follows: -10 min=405 pg/mL, - 5 min=404 pg/mL, + 2 min=3201 pg/mL, + 5 min=3439 pg/m, +10 min=2445 pg/mL, +20 min=1218 pg/mL, +30 min=578 pg/mL. He was diagnosed with gastrinoma based on the SST results. Genetic testing did not show any pathogenic sequence variants or deletions/duplications identified in MEN-1; CASR; CDC73; CDKN1B or RET. Given history of hyperparathyroidism and gastrinoma, he was clinically diagnosed with MEN1 syndrome. Ga-68 DOTATATE scan in May 2019 revealed focal radiotracer avidity in the tail the pancreas suspicious for neuroendocrine tumor and multiple radiotracer avid retroperitoneal and abdominal lymph nodes. Focal radiotracer avid lesion was also noted in the sacrum suspicious for osseous metastatic disease. He was started on lantreotide monthly injections in July 2019. Gastrin level decreased to 94 pg/mL 1 week after first injection, however later increased to 304 pg/ml 1 week after third dose of lantreotide. Surgical options are also being explored.Conclusion:An increase in more than 120pg/mL over basal gastrin level within 10 min in SST is consistent with a diagnosis of gastrinoma. Our patient demonstrated an impressive increase in gastrin level with SST while on PPI therapy. Pertinent diagnostic information was successfully obtained without increasing the risk of complications that can occur by withdrawal of PPI therapy.

Case report: optimal tumor cytoreduction and octreotide with durable disease control in a patient with MEN-1 and Zollinger-Ellison syndrome\u2014over a decade of follow-up

BackgroundZollinger-Ellison syndrome (ZES) is a rare condition characterized by hypersecretion of gastrin by gastrinoma tumors leading to severe peptic ulcer disease with potential development of gastric carcinoid tumors. Herein, we report the clinical course of a 68-year-old patient with multiple endocrine neoplasia type 1 (MEN-1) who underwent several surgeries to ultimately undergo optimal tumor cytoreduction of locally advanced gastrinomas and symptomatic gastric carcinoids. The patient was subsequently maintained on octreotide long-acting release (LAR). This case report supports consideration for aggressive tumor cytoreduction and octreotide in similar patients with MEN-1-associated ZES for durable disease control and symptom management.Case presentationThe patient is a 68-year-old male with multiple endocrine neoplasia type 1 (MEN-1), diagnosed in 1993 after presenting with recurrent renal calculi and hypercalcemia. Soon thereafter, he presented with symptoms and elevated gastrin levels suggestive of ZES prompting abdominal exploration with partial resection of the duodenum to remove gastrinoma tumor nodules. Within 4 years of the operation, he represented with intractable hypergastrinemia despite optimal medical management with peak gastrin levels exceeding 29,000 pg/mL, in 2006. In January 2007, the patient returned to the operating room for resection of regional peripancreatic and perigastric lymph nodes and enucleation of pancreatic body and tail gastrinoma tumors. Although his gastrin level decreased to 5000 pg/mL with resultant improvement of symptoms, in less than 2 years, he developed disease progression with obstructive symptomatology from enlarging gastric carcinoids and rising gastrin levels. In May of 2008, he underwent pancreaticoduodenectomy and near-total gastrectomy. Since June of 2008, the patient shows no demonstrable progression of disease and remains asymptomatic on LAR octreotide (30 mgs). Gastrin levels have been well controlled (range, 100–624 pg/mL; current 114 pg/mL).ConclusionSuccess of this procedure in our case report highlights the potential role for optimal tumor cytoreduction and LAR octreotide to control disease progression in a patient with MEN-I and Zollinger-Ellison syndrome with locally advanced gastrinoma and secondary large gastric carcinoids.

Signet Ring Cell Carcinoma Masquerading as Severe Peptic Ulcer Disease

Signet Ring Cell Carcinoma Masquerading as Severe Peptic Ulcer Disease

Assessing for Multiple Endocrine Neoplasia Type 1 in Patients Evaluated for Zollinger-Ellison Syndrome—Clues to a Safer Diagnostic Process

BackgroundZollinger-Ellison syndrome is a rare cause of tumoral hypergastrinemia; 1 of 5 patients with this syndrome also has multiple endocrine neoplasia type 1. The diagnosis of this disease is complicated by the widespread use of proton pump inhibitors that can elevate serum gastrin levels, the cornerstone for biochemical diagnosis. Abrupt discontinuation of proton pump inhibitors could lead to adverse outcomes. Clinician awareness of the relationship between Zollinger-Ellison syndrome and multiple endocrine neoplasia type 1 could lead to a safer diagnostic pathway. MethodsWe conducted a retrospective review of a cohort of patients with multiple endocrine neoplasia type 1. ResultsThere were 287 patients with multiple endocrine neoplasia type 1 (73 with gastrinoma) evaluated between 1997 and 2014. Two patients experienced adverse events after proton pump inhibitor therapy was discontinued to re-measure serum gastrin level during the evaluation of severe peptic ulcer disease. In both cases, the diagnosis of multiple endocrine neoplasia type 1 was made after proton pump therapy was discontinued. ConclusionAbrupt discontinuation of proton pump therapy can lead to adverse outcomes in patients with Zollinger-Ellison syndrome. Clinical assessment for features of multiple endocrine neoplasia type 1 (eg, serum calcium levels, personal and family history of hypercalcemia, pituitary or pancreatic tumors) could identify patients with higher risk for a tumoral source of hypergastrinemia where imaging studies can help support the diagnosis without the potential side effects of abrupt discontinuation of proton pump inhibitor therapy.

Can We Repackage Omeprazole Capsules Into Multicompartment Compliance Aids?

Can We Repackage Omeprazole Capsules Into Multicompartment Compliance Aids?

Sporadic duodenal macrogastrinoma: a rare case report

Gastrinomas are rare neuroendocrine tumors characterized by the secretion of gastrin, which causes hyperchlorhydria, thereby producing the Zollinger-Ellison syndrome. In most cases this syndrome manifests as severe peptic ulcer disease. We are presenting an extremely rare clinical case of sporadic duodenal macrogastrinoma. The patient underwent investigation due to six-year history of epigastric pain, heartburn and episodic diarrhea. Endoscopy, endosonoscopy and histologic examination of biopsy specimens indicated the presence of duodenal gastrinoma with no signs of peptic ulcers. Pyloroduodenal segment including 3.5 cm macrogastrinoma was resected. This case is unique as duodenal gastrinomas are usually very small, up to 1 cm. During the follow up period we observed slowly decreasing hypergastrinemia. Somatostatin receptor scintigraphy, CT and upper GI endoscopy were performed to reveal the reasons, though did not find any abnormalities. 8 months of follow-up did not reveal any progression of the disease. The etiology of slowly decreasing hypergastrinemia remains unclear, controversial and is under investigation.

Article Commentary: Zollinger–Ellison Syndrome: A Personal Perspective

The odyssey of Zollinger-Ellison Syndrome is one of the most interesting in surgery. From the initial recognition of two patients with severe peptic ulcer disease in 1955 sprung an international dialogue on this unique disease culminating in discovery that gastrin was the hormone secreted by these pancreatic and duodenal tumors. The impact was the birth of a new area of science, "gastrointestinal endocrinology." Initially, surgeons were challenged by the complexity of the patients and the need to perform total gastrectomy to prevent death from complications of the severe ulcer disease. Later, after the discovery of proton pump inhibitors, total gastrectomy was no longer needed and the surgeon could focus treatment on tumor removal added by radioimmunoassay for gastrin and new imaging modalities. Today, we recognize that all gastrinomas have malignant potential; early surgical removal can reduce the incidence of metastases and improve survival, independent of biochemical cure, in both sporadic and familial forms of the disease.

Exposure to nonsteroidal anti-inflammatory drugs among older adult patients hospitalized for peptic ulcer disease in Argentina: A case-control study

Objectives: This study examined the association between exposure to nonselective NSAIDs and hospitalization for peptic ulcer disease (PUD) among older adults in Argentina. Methods: This was a case-control study based on the medical records of 5 hospitals in Buenos Aires. Cases were patients aged ≥50 years and hospitalized with PUD between 1997 and 2002 who were identified by mode of presentation (acute abdominal pain, vomiting, hematemesis, melena, shock, and asymptomatic anemia, or admission for an unknown reason and a discharge diagnosis related to upper gastrointestinal complications). Controls were hospitalized patients without PUD and were matched to cases (1:1) by age, sex, and admission date. NSAID exposure was defined as the use of NSAIDs during the year before admission. Conditional logistic regression analysis was used to examine the association between exposure to nonselective NSAIDs and hospitalizations for PUD, after adjusting for predictors. Subgroup analyses were conducted on patients with severe PUD, moderate PUD, and those whose PUD was confirmed by endoscopy. Results: The study included 324 cases and 324 matched controls. The mean patient age was 74 years. The discharge diagnoses indicated severe PUD in 46.3% (150/324), moderate PUD in 49.4% (160/324), and mild PUD in 4.3% (14/324) of cases. NSAID exposure was associated with an increased risk of hospitalization for PUD (odds ratio [OR], 5.20; 95% CI, 3.31–8.15). Risk was also increased for severe PUD (OR, 4.24; 95% CI, 2.29–7.87) and moderate PUD (OR, 6.08; 95% CI, 3.09–11.96). A history of upper gastrointestinal complications was independently associated with hospitalization for PUD (OR, 14.62; 95% CI, 6.70–31.91). Conclusions: Use of nonselective NSAIDs is a significant risk factor for PUD-related hospitalizations among older adults in Argentina. The magnitude of the risk ratio resembles that reported for developed countries.

Severe Ataxia, Myelopathy, and Peripheral Neuropathy Due to Acquired Copper Deficiency in a Patient With History of Gastrectomy

In animal studies, copper absorption has been demonstrated to occur in the proximal gut via duodenal enterocytes. Acquired copper deficiency is known as "swayback" in ruminant animals and Menkes' disease in humans. Copper is an essential micronutrient necessary for the hematologic and neurologic systems. Acquired copper deficiency in humans has been described, causing a syndrome similar to the subacute combined degeneration of vitamin B(12) deficiency. This is a single case report. Our patient developed a neurologic constellation of ataxia, myelopathy, and peripheral neuropathy similar to vitamin B(12) deficiency many years after gastrectomy for severe peptic ulcer disease. The patient was maintained for decades with enteral feedings via jejunostomy that provided the recommended dietary allowance (RDA) for copper. Copper deficiency was suspected, identified, and treated. Over 3 months of follow-up, serum copper levels increased from 4 microg/dL to 20 microg/dL (70-150 microg/dL), and ceruloplasmin increased from 6 mg/dL to 8 mg/dL (14-58 mg/dL). During this short time of follow-up, the patient has had no further progression of his neurologic symptoms. Ataxia and myelopathy secondary to acquired copper deficiency are rare complications of major gastric resection. This is quite similar to the syndrome of vitamin B(12) deficiency. Vitamin B(12) repletion does not improve symptoms. Bariatric procedures such as gastric bypass surgery result in a similar functional anatomy of the proximal gut and may place more patients at increased risk. Early recognition and therapy with oral or parenteral copper may lead to a decrease in both neurologic and hematologic consequences.

Pantoprazole in severe acid-peptic disease: the effectiveness and safety of 5 years’ continuous treatment

Objective. This is our final report on the clinical effectiveness and safety of long-term pantoprazole in patients with severe peptic ulcer or reflux disease during continuous treatment for up to 5 years. Methods. Patients ( n = 150) with peptic ulcer or reflux erosive oesophagitis running an aggressive course or with complications, and refractory to H2-receptor antagonists, were entered into this 5-year programme. Assessment was by serial endoscopy, clinical examination, serum gastrin estimation, gastric mucosal histology and mucosal endocrine cell quantification. Results. Healing results were presented earlier. The estimated rates of remission on maintenance treatment with pantoprazole ( n = 115) were 82% at 1 year, 75% at 2 years, 72% at 3 years, 70% at 4 years and 68% at 5 years. Helicobacter pylori infection appeared not to influence the outcome in reflux patients, with roughly two-thirds continuing in remission irrespective of infection. Only four patients had adverse events considered to be definitely related to pantoprazole. Median gastrin levels rose by 1.5–2-fold and were higher in those with H. pylori infection; 13 patients had levels >500 ng/L on at least one occasion, but these high levels were not sustained. Histological changes were more marked in patients infected with H. pylori: chronic gastritis decreased in the antrum and increased in the corpus, which also showed atrophic changes. The total number of endocrine cells in the antrum showed little variation over 60 months but fell by around one-third in the corpus. Conclusion. Long-term treatment with pantoprazole is effective and safe.

Continuous maintenance therapy with omeprazole for more than 10 years in patients with severe peptic ulcer or reflux esophagitis disease (13–17 years)

continuous maintenance therapy with omeprazole for more than 10 years in patients with severe peptic ulcer or reflux esophagitis disease (13–17 years)

Continuous maintenance therapy with omeprazole for more than 10 years in patients with severe peptic ulcer or reflux esophagitis disease (13–17 years)

continuous maintenance therapy with omeprazole for more than 10 years in patients with severe peptic ulcer or reflux esophagitis disease (13–17 years)

Immediate repeat course of amoxycillin, metronidazole and omeprazole to eradicate Helicobacter pylori

To investigate a repeat treatment regimen with the same antibiotic combination of amoxycillin and metronidazole in patients with continuing Helicobacter pylori infection. Eighty-two patients with severe peptic ulcer disease and concurrent Helicobacter pylori infection were treated with a two week regimen of omeprazole (40 mg once daily), amoxycillin (750 mg t.d.s.) and metronidazole (400 mg t.d.s.). Upper gastrointestinal tract endoscopy was performed before, and approximately 2 months after, completion of antibiotic therapy. Biopsies were taken for rapid urease testing and the histological demonstration of H. pylori infection. Patients with persistent H. pylori infection at follow-up endoscopy were re-treated with a second and identical antibiotic treatment course. A subsequent endoscopic examination with accompanying biopsies was performed at least 6 weeks after the second treatment course and after a further 6, 18 and 30 months. Eradication of H. pylori was achieved in 69 patients (84%, 95% CI: 75-90%) after the first treatment. Four patients (4/82 = 5%) were withdrawn from the study because of side-effects. All of the remaining nine patients had their H. pylori infection eradicated after the second treatment course (95% CI: 70-100%). Seventy-eight patients had a follow-up examination after a median 30 months of the initial eradication of H. pylori, and all but one remained free of infection and none had an ulcer relapse. This study demonstrates that patients with persistent H. pylori infection after completing a primary course of omeprazole (40 mg once daily), amoxycillin (750 mg t.d.s.) and metronidazole (400 mg t.d.s.) will probably respond to a repeat course of treatment with the same antibiotic combination.

Endocrine Tumors of the Small and Large Intestine

Among endocrine tumors arising in the intestinal tract, midgut argentaffin EC cell carcinoids, duodenal gastrin cell tumors and rectal trabecular L cell carcinoids, in order of decreasing frequency, are those better represented. Together they account for more than 80% of such tumors. Duodenal somatostatin cell tumors, gangliocytic paragangliomas and poorly differentiated neuroendocrine carcinomas, are also well defined tumor entities. The carcinoid syndrome with intermittent flushing, hypotension and diarrhea, and the Zollinger-Ellison syndrome with severe peptic ulcer disease, are the only hyperfunctional syndromes consistently found in association with these tumors. The carcinoid syndrome arises in about 10% of intestinal carcinoids, usually in their advanced metastatic stage. The Zollinger-Ellison syndrome occurs in association with about 40% of gastrin cell tumors, including small intramural growths. Tumor prognosis depends on mode and site of presentation, histology, cell type(s), size, level of invasion, metastases (especially distant metastases) and associated clinical syndrome or background disease.